ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Angiotensin II-mediated posttranslational modification of nNOS in the PVN of rats with CHF: role for PIN.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- The brain-heart axis: effects of cardiovascular disease on the CNS and opportunities for central neuromodulation.Nature reviews. Neuroscience · 2026Review
- Degradation of nNOS in the PVN of Rats With Heart Failure: Role of CHIP.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Downregulation of neuronal nitric oxide synthase (nNOS) within the paraventricular nucleus in Ins2Nitric oxide : biology and chemistry · 2025Article
- Article
- Angiotensin II inhibits the A-type KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Central Ang II (Angiotensin II)-Mediated Sympathoexcitation: Role for HIF-1α (Hypoxia-Inducible Factor-1α) Facilitated Glutamatergic Tone in the Paraventricular Nucleus of the Hypothalamus.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Central angiotensin II-Protein inhibitor of neuronal nitric oxide synthase (PIN) axis contribute to neurogenic hypertension.Nitric oxide : biology and chemistry · 2020Article
- Vasopressin & Oxytocin in Control of the Cardiovascular System: An Updated Review.Current neuropharmacology · 2020Review
- Exercise training augments neuronal nitric oxide synthase dimerization in the paraventricular nucleus of rats with chronic heart failure.Nitric oxide : biology and chemistry · 2019Article
- GABA-containing liposomes: neuroscience applications and translational perspectives for targeting neurological diseases.Nanomedicine : nanotechnology, biology, and medicine · 2018Review
- Superoxide Anions and NO in the Paraventricular Nucleus Modulate the Cardiac Sympathetic Afferent Reflex in Obese Rats.International journal of molecular sciences · 2017Article
- Carotid Body-Mediated Chemoreflex Drive in The Setting of low and High Output Heart Failure.Scientific reports · 2017Article
- A novel role for miR-133a in centrally mediated activation of the renin-angiotensin system in congestive heart failure.American journal of physiology. Heart and circulatory physiology · 2017Article
- Constitutive NOS uncoupling and NADPH oxidase upregulation in the penis of type 2 diabetic men with erectile dysfunction.Andrology · 2017Article
- Post-translational regulation of neuronal nitric oxide synthase: implications for sympathoexcitatory states.Expert opinion on therapeutic targets · 2017Review
- Astrocytes Contribute to Angiotensin II Stimulation of Hypothalamic Neuronal Activity and Sympathetic Outflow.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Central Angiotensin-II Increases Blood Pressure and Sympathetic Outflow via Rho Kinase Activation in Conscious Rabbits.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Liposome-entrapped GABA modulates the expression of nNOS in NG108-15 cells.Journal of neuroscience methods · 2016Article
- Sympathoexcitation in Rats With Chronic Heart Failure Depends on Homeobox D10 and MicroRNA-7b Inhibiting GABBR1 Translation in Paraventricular Nucleus.Circulation. Heart failure · 2016Article
- Brain mechanisms of sympathetic activation in heart failure: Roles of the renin‑angiotensin system, nitric oxide and pro‑inflammatory cytokines (Review).Molecular medicine reports · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
An increased sympathetic drive is an adverse characteristic in chronic heart failure (CHF). The protein expression of neuronal nitric oxide synthase (nNOS)- and hence nitric oxide (NO)-mediated sympathoinhibition is reduced in the paraventricular nucleus (PVN) of rats with CHF. However, the molecular mechanism(s) of nNOS downregulation remain(s) unclear. The aim of the study was to reveal the underlying molecular mechanism for the downregulation of nNOS in the PVN of CHF rats. Sprague-Dawley rats with CHF (6-8 wk after coronary artery ligation) demonstrated decreased nNOS dimer/monomer ratio (42%), with a concomitant increase in the expression of PIN (a protein inhibitor of nNOS known to dissociate nNOS dimers into monomers) by 47% in the PVN. Similarly, PIN expression is increased in a neuronal cell line (NG108) treated with angiotensin II (ANG II). Furthermore, there is an increased accumulation of high-molecular-weight nNOS-ubiquitin (nNOS-Ub) conjugates in the PVN of CHF rats (29%). ANG II treatment in NG108 cells in the presence of a proteasome inhibitor, lactacystin, also leads to a 69% increase in accumulation of nNOS-Ub conjugates immunoprecipitated by an antiubiquitin antibody. There is an ANG II-driven, PIN-mediated decrease in the dimeric catalytically active nNOS in the PVN, due to ubiquitin-dependent proteolytic degradation in CHF. Our results show a novel intermediary mechanism that leads to decreased levels of active nNOS in the PVN, involved in subsequent reduction in sympathoinhibition during CHF, offering a new target for the treatment of CHF and other cardiovascular diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.